Work in this laboratory indicates that the edema associated with experimental heart failure produced by thoracic caval constriction in dogs is associated with an elevated water intake which is dependent on high angiotensin levels. Increased thirst has also been observed in renal hypertension. Fluid restriction allieviated the edema. The objective of the present study is to follow up and to extend these observations to assess the contribution that increased fluid intake, and retention of the extra fluid, makes to the etiology of the edema. The effects of graded fluid restriction, and of pharmacological suppression of the increased thirst drive, on the development of edema will be assessed. The experiments will be extended to dogs with experimental valve lesions, such as mitral stenosis, which also lead to congestive heart failure. The role of a possible increase in salt appetite will also be assessed. Measurements will be made of fluid and electrolyte balance, plasma renin activity, plasma angiotensin II, vasopressin and ACTH concentration. In some experiments, cardiac function will also be assessed.